The American cutaneous forms of leishmaniasis include Venezuela. immune-responder individuals with localised cutaneous leishmaniasis (LCL) and non-responder individuals with diffuse cutaneous
leishmaniasis (DCL). Patients with intermediate or chronic cutaneous
leishmaniasis (ICL) have increased morbidity due to the length of their illness, atypical forms and areas of compromise. In the present study, we evaluated the expression of the leukocyte antigens (CD4, CD8, CLA:
cutaneous lymphocyte antigen, CD69, CD83 and CD1a) and cytokines (IFN-g, IL-4, IL-10 and TGF-b1) in the lesions of patients with ICL (n½18) using an immunocytochemical procedure. ICL results were compared with the information for LCL (n½19) and DCL (n½4). The numbers of CD4¹ and CD8¹ T cells in ICL were similar to those of LCL lesions, but significantly different (P#0.05) from DCL lesions. LCL lesions have about half the numbers of early activated CD69¹ cells as ICL, but most are CLA¹ skin homing memory T cells, whereas ICL lesions have the
highest number of CD69¹ T cells, but about one-third of these cells expressed CLA. This suggests that the granuloma of ICL patients
contains many activated T cells that are unprimed to cutaneous-launched antigens, thus contributing to an aberrant immune response. In contrast, DCL granulomas presented the lowest numbers of activated CD69¹ and
CLA¹ cells, associated with the characteristic tolerogenic state of these
patients. The immunolocalisation of cytokines showed a mixed cytokine pattern in ICL lesions with many positive cells for IL-10, TGF-b1, IL-4 and IFN-g, with a preponderance of the first two, and different from the responses associated with LCL and DCL lesions, cutaneous leukocyte antigen – cytokine pattern – respectively. CD1a¹ Langerhans cells were decreased (P#0.05) in both ICL (271º15 cells/mm2) and DCL (245º19 cells/mm2) as compared to immunophenotypes
LCL (527º54 cells/mm2) epidermis. The percentage of IL-10¹ epidermal Langerhans cells in ICL (33.69), from the total CD1a¹ population, was higher than in LCL (17.45). In addition, fewer CD83¹ primed Langerhans cells were present in ICL epidermis. The diminished participation of epidermal Langerhans cells, causing a defective signalling by the epidermis, in ICL lesions may account for the tissue-damaging state observed in these patients.